The hypothesis of this project is that an increase in uterine artery vasodilator production is associated with a marked increase in AT1-R expression and/or coupling of existing AT1-R in uterine artery endothelial cells. Aim 1 is to investigate, using 5-RACE cloning + RT/PCR assays, if there are pregnancy-specific isoforms of AT1-R mRNA in uterine artery endothelial cells. Aim 2 is to establish in vivo that pregnancy-induced changes in AT1-R expression are due to direct or indirect, via bFGF or VEGF, actions of estrogen. Aim 3 is to determine in vitro whether changes in expression result from changes in phospholipase C and PGI2 production.